It is clearly established that during development young animals and humans maintain a positive sodium balance, which is required for continued growth and the preservation of homeostasis. Multiple studies have demonstrated that only a small fraction of the dietary sodium is excreted into the urine of growing subjects, even when the diet is so excessively rich in sodium that clinically apparent edema develops. Recent evidence suggests that a high distal tubular reabsorption of sodium is, in part, responsible for the normal positive balance and the limited natriuresis observed following sodium expansion. The plasma renin activity and serum aldosterone concentration have also been shown to be high in normal neonates; however, the role of these substances in determining the positive sodium balance and limited excretory capacity has not been tested. In addition, the mechanisms by which the renin-angiotensin-aldosterone system is kept at a high level have not been studied. We propose to test the role of the renin-angiotensin system in determining the pattern of sodium homeostasis during development by blocking the conversion of angiotensn I to antiotensin II and measuring sodium excretion. The integrity of the renin-angiotensin-aldosterone system will be investigated using a excretion. The integrity of the renin-angiotensin-aldosterone system will be investigated using a similar blockade or suppression of renin release by saline loading and measuring the plasma aldosterone concentration. The mechanism controlling the release of renin will be studied by measuring plasma renin after altering renal perfusion pressure in a non-filtering kidney model, as well as after increasing the delivery of sodium to the macula densa area while renal perfusion pressure is held constant. Finally, we propose to test the influence of the distribution of the body fluids on sodium excretion and renin activity by measuring each of them before and after selective expansion of different compartments.